四分位间距
炎症
医学
全身炎症
生理学
肺
内科学
免疫学
作者
Shizhen He,Björn Lundberg,Jenny Hallberg,Susanna Klevebro,Göran Pershagen,Kristina Eneroth,Erik Melén,Matteo Bottai,Olena Gruzieva
标识
DOI:10.1016/j.ijheh.2023.114294
摘要
Systemic inflammation is one potential mechanism underlying negative impact of air pollution on lung function. Levels of inflammation-related proteins have the potential to characterize infants' susceptibility to air pollution induced lung function impairment. This study aimed to examine the interplay between air pollution exposure and inflammation-related proteins on lung function in 6-months-old infants.In the EMIL birth cohort from Stockholm (n = 82), dynamic spirometry, along with measurement of plasma levels of 92 systemic inflammation-related proteins (Olink Proseek Multiplex Inflammation panel) have been carried out in infants aged six months. Time-weighted average exposure to particles with an aerodynamic diameter of <10 μm (PM10), <2.5 μm (PM2.5), and nitrogen dioxide (NO2) at residential addresses from birth and onwards was estimated via validated dispersion models. To characterize the abnormality of inflammation-related protein profile, for each protein in each infant, we calculated the relative deviance of the protein level from age- and sex-specific median in terms of its age- and sex-specific interquartile range (IQR), followed by computing the absolute value of the smallest relative deviance, "minimum absolute deviance". Using linear regression models, interaction of air pollution and the abnormal inflammatory profile on lung function was estimated on the additive scale.We found joint association of PM exposure and an abnormal inflammatory protein profile in relation to FEV0.5 and FVC. For 0.1 unit increase in minimum absolute deviance, one IQR increase in PM10 was associated with 85.9 ml (95% CI: -122.9, -48.9) additional decrease in FEV0.5, and 72.3 ml (95% CI: -121.5, -23.2) additional decrease in FVC. Similar results were obtained with PM2.5 exposure, while less apparent for NO2.Early life air pollution exposure and abnormal inflammation-related protein profiles may interact synergistically towards lower lung function in infants.
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